The fungal viruses exhibit a number of properties that make them attractive material for molecular genetics. Their most unique characteristic is their almost universal lack of an infectious cycle (hence the prediliction among some to cal them plasmids). Presumably, this failing of the fungal viruses is the result of the intractable fungal cell wall. Rising above their inability to propagate themselves by infection, the fungal viruses have made rather remarkable adaptations to their permanent residence in host cells. The yeast virus, for instance, requires numberous host functions for its very survival. The yeast and Ustilago viruses have both adopted one of the strategies of plasmids: that is,. to make toxins fatal to cells not harboring virus particles. It is because of this property that the yeast and Ustilago systems are amenable to genetic analysis. All the well-documented fungal viruses are double-stranded RNA (dsRNA) viruses. The two virus systems susceptible to genetic analysis (yeast and Ustilago) are very similar: both exhibit defective interfering particles and virus exclusion; both have a single large capsid protein encoded by a large viral dsRNA; both have toxin polypeptides of about 11,000 daltons synthesized as prepolypeptides of larger size and encoded by dsRNAs of about 1 kilobase pairs (1kpb). We would like to apply the same methods used to elucidate the relationships among the yeast viral dsRNAs (heteroduplex mapping and 3' end sequencing) to the more complicated Ustilago system. These experiments should enable us to understand exclusion of some viruses by others, to map the capsid polypeptide coding region on its dsRNA(s), to determine the evolutionary relationships between two different fungal viruses. We should then be able to make some general statements about those properties essential to dsRNA viruses capable of indifinite "persistent infection."